Animals are getting fatter, too

Is something in the environment making everyone -- animals and humans -- gain weight?

By Carrie Arnold | November 24, 2010

Obesity levels have risen dramatically in research animals and others living close to humans, suggesting environmental factors are encouraging everyone to gain weight, according to new findings in the linkurl:Proceedings of the Royal Society B.;http://rspb.royalsocietypublishing.org/content/early/2010/11/19/rspb.2010.1890.abstract

"These results show that the obesity epidemic is not as simple as people might think," said linkurl:Jennifer Kuk,;http://www.yorku.ca/health/people/index.php?dept=K&mid=645785 a biologist who studies obesity at York University in Canada and was not involved with the study.
It's no secret that obesity has become an epidemic in humans -- among American adults, nearly one in three is obese, defined as having a Body Mass Index (BMI) greater than 30. Researchers have pointed their fingers at everything from a lack of physical activity to the highly processed foods that so many of us eat.
But what if something in the environment was at least partly to blame, as well? To investigate, linkurl:David Allison,;http://www.soph.uab.edu/ssg/people/davidallison a statistical geneticist at the University of Alabama, Birmingham, and his colleagues gathered data on body weights of more than 20,000 adult animals from 24 populations of 8 different species from around North America. The authors included only those mammals for which there were two weight measurements in the past 50 years, and whose weight was not deliberately manipulated as part of research or a livestock feeding program.
All 24 populations of animals, which ranged from primates housed in research facilities to feral rats living in the greater Baltimore area, showed significant increases in body weight. Average body weights of captive chimpanzees increased at a rate of 33 percent each decade, and 9 percent per decade in captive marmosets. Laboratory mice got 12 percent fatter every ten years, laboratory rats did by 3 percent; the average body mass of Baltimore's feral rats increased by almost 7 percent each decade. And house pets were no exception, either. The average weight of cats increased by almost 10 percent each decade, while dogs' weights increased by 3 percent every decade.
Not only did body weight increase significantly, but so did the chances than an animal would be obese. In 23 out of the 24 populations, animals were more likely to be obese -- defined as weight above the 85th percentile at the initial time-point -- at the second time-point than at the first.
What's more, the increased body weights and increased likelihood of obesity were found even in animals whose diets and physical activity levels were known to be the same throughout the study period. So if dietary changes and energy imbalance weren't responsible for the rise in obesity, said Allison, it may be some environmental factor.
"If we're seeing these trends in other mammals, it shows that there must be another explanation" besides the main culprits of inertia and poor diet, Kuk said.
Of course, some animals -- such as research animals -- could be eating more and exercising less just as we are. Allison acknowledged that this is likely possible, but noted that scientists have records of exactly what research animals were fed, and housing conditions haven't changed much in the past 50 years.
Environmental toxins and viruses are at the top of Allison's list of potential suspects. Several studies have linked endocrine disruptors such as bisphenol A (BPA) and some tin-containing compounds to increased body mass. Infections by viruses, specifically a type of the common cold-causing adenovirus, have also been linked to significantly increased body mass.
"We've got to really open our minds to thinking about some other things," Allison said. He emphasized that diet and exercise are still key factors in why people and animals gain weight, but "we clearly now have evidence that things outside this realm can shift the body weight distributions of an entire population."
Klimentidis Y, et al. "Canaries in the coal mine: a cross-species analysis of the plurality of obesity epidemics." Proc R Soc B. linkurl:doi: 10.1098/rspb.2010.1890;http://rspb.royalsocietypublishing.org/content/early/2010/11/19/rspb.2010.1890.abstract **__Related stories:__***linkurl:Rat dad's diet affects pups;http://www.the-scientist.com/news/display/57757/ [20th October 2010] *linkurl:Same poop, different gut;http://www.the-scientist.com/news/display/57795/ [3rd November 2010] *linkurl:Eat your way to better DNA;http://www.the-scientist.com/article/home/24535/ [1st September 2006]

Advertisement

Comments

Wager: Increased food consumption by Humans trickles down to pets, pests and other animals that live with and around us.\nA good control would be to look at the same domestic and feral animals in less fat countries (China, Europe vs US).\n\nThe ultimate cause is most likely due people eating, trashing and feeding at an increasing rate.

It is not clear if environmental toxins and viruses are responsible for obesity in humans and domesticated animals. As noted by jonathan bohbot it needs a study that compares same species of animals in domestic settings and wild. Common sense tells availability of plenty of food all the times and sedentary life style are the major culprits. Sure preservatives added in processed foods need close attention.

We feed food animals chemicals that make them grow quicker and fatter. Are there residues of these chemicals in the food we eat and in what we feed companion animals. Non therapeutic use of antibiotics or other antimicrobials? Other supplements?

Allergic response to particulates, specifically 2.5, might have something to do with it?\nI'm a biologist who has studied the inflammation caused by pm 2.5. And believe that not just heart disease, diabetes, and stroke are triggered.

Come on folks , I do not believe that the main stream refuses to accept the fact of obesity is mainly caused by eating what is offered as good, healthy food but it is NOT! Processed food for the last 10,000 years or so is when all our health problems started . The age of agriculture makes edible food that as a whole would be indigestible for us. If you cannot use it you should not be eating it. ONLY whole foods as nature provides will sate appetites and stop the binge easting caused by the carbs( sugar) content in our S.A.D.\nBefore agriculture our hunter/gatherer forebears were taller , had larger brains and suffered none of the modern diseases that plague the peoples today.

Both fluoride and chlorine are goitrogenic. Then you add in that they are going to be eating, amonst other environmental toxins, GM grains and grain products. Those poor animals just don't have a chance.

Human-prepared foods, even those that appear on the surface to be "the same", have changed dramatically due to the changes in the ingredients during the study period, so even in those animals whose diets were "the same" during the study period, e.g. the lab animals with unrestricted access to chow, the two measures aren't comparable. For example, in lab animal chow or in the human foods that rats (both urban and rural, but especially urban) consume, the use of ingredients such as hydrogenated oils and high-fructose corn syrup has probably increased during the study period, even though the end-product and consumption rate remained "the same". It would be interesting to see a study of animals, e.g. lab animals, comparing their reactions to natural food sources (raw whole foods) versus processed/human-made foods, and also to look at other measures of health apart from weight alone. But this is an interesting paper nonetheless.

if energy input (carbs+protein)is equal to energy output then you have balance.\nif energy input is exceded by output you have obesity.\nif energy input is less than energy output you have anoxeia.\nit does not take Einstien to figure this out. \nBarbara from Oz\n

The earth is passing through a force field in our sector of the galaxy that suppresses metabolism. It also depresses intelligence, leading to an increase in bad science and blogging. Ooh, here comes that headache again.

Experimental design:\nfeed two rodent dams a normal diet during pregnancy, but spike one of the dam's diets with synthetic estrogen (DES, BPA, ...). Their offspring get the same TYPE and AMOUNT of food but one of them is obese as adult--the one exposed to xenoestrogen during fetal development. There is scientific evidence for obesogen-caused overweight so what's so hard to accept about this? Of course other factors play a role: what you eat, how much you eat, how much you excercise, maybe even when you eat and how much you sleep, but clearly chemicals (obesogens) do play a role. Instead of denying this we should start researching why.

We have been trying to find the other causes of obesity besides the obvious, and observing that animals have the same trends narrows down the possible causes. \nI remember a researcher observing that the pattern of spread of obesity resembles the spread of a retrovirus. Congragulations to the author for this useful observation, and I hope followup is done on these findings.

Your article on animals are getting fatter is quite interesting, because obesity may be adiseases of the brain which may be due to decreased intake of w-3 and increased intake of w-6 fat in the diet. Obesity and type 2 diabetes mellitus have become major health problems in both developing and developed countries. The exact pathogenesis of obesity and type 2 diabetes mellitus that are components of metabolic syndrome is not known.\nPhysical inactivity and increased intake of energy in association with gene expression are common predisposing factors for obesity and metabolic syndrome. Apart from these factors, brain-related mechanisms concerned with the hypothalamus and vagus nerve have been implicated in such pathogenesis. The role of liver and beta cells of the pancreas and their interactions with the hypothalamus and vagus nerve are important mechanisms to explain the behavioural factors in the pathogenesis of obesity and metabolic syndrome. It seems that a neuronal pathway consisting of the afferent vagus from the liver and efferent sympathetic nerves to adipose tissues appear to be involved in the regulation of energy expenditure, systemic insulin sensitivity, glucose metabolism, and fat distribution between the liver and the peripheral tissues. Therefore, it is likely that the liver conveys information regarding energy balance to the brain via the afferent vagus, whereas leptin could be a humoral signal to the brain from the adipocytes. It is possible that the brain receives information from several tissues and organs via both humoral and neuronal pathways, which it integrates to produce an appropriate response; sympathetic nervous system activation and or parasympathetic modulation to maintain energy homeostasis. In this connection, the role of w-6/w-3 fatty acids ratio on liver-pancreas and brain function in relation to the Tsim Tsoum concept appears to be very interesting because it places emphasis on mind-body connection/interactions in the pathogenesis of obesity and diabetes. Omega-3 fatty acids can also improve neuronal efficiency causing improvement in attention, cognitive performance, mood-state and in the electroencephalographic alpha and theta oscillations which are indicators of memory function. Treatment of type 2 diabetes mellitus and coronary atherosclerosis with an ω-3 fatty acid rich Mediterranean diet may be protective by their direct effect as well as by their influence on the hypothalamic and vagal connections. Brain derived neurotrophic factor has also been found to decreased obesity and blood glucose.\nIn brief, it is possible that liver and pancreas via vagus nerve and hypothalamic connections as well as via humoral mechanisms can influence energy metabolism and food intake to maintain energy homeostasis which may have an independent effect on the development of obesity, type 2 diabetes and metabolic syndrome. A high W-8/W-3 fatty acids ratio in the diet can damage the gut-liver-brain axis and may also have an independent effect on liver-pancreatic beta cells and brain connections leading to obesity and metabolic syndrome.\nRBSingh,MD, Fabien De Meester,PhD, Agnieszka Wilczynska,PhD, DW Wilson,PhD\nTsim Tsoum Institute, Krakow,Poland\n\n

The comment about oestrogen is interesting.I am told that Soy products contain phytoestrogens.I was surprised when a friend and myself checked processed food items in the supermarket, just how many products contain soy and it's derivatives- it would appear that the only way to avoid it is to eat only fresh unprocessed foods.

Scientist need to figure out what food and Drug administrative is lacking in implementing only because they do not have good scientific data to backup them up. Example What food additives or process food is not non-reactive inside human body and hence cannot be process or process completely or properly due to which toxins accumulation becomes more common, which causes lack of energy, which causes one to eat more food and the cycle goes spiraling down..... and I would like to add that I disagree with comments from barbara vincent regarding more intake and less output of energy theory. There is no scientific evidence on that in fact there are many examples found by Dr A.T.W clearly documented that people who eat very little and do lot of physical work have obese tendencies. Obesity has nothing to do with Environmental factors unless somebody proves that obesity is contagious by presence of something in the external environment.

This article is interesting but what evidence is there that this is anything more than a correlation? There doesn't seem to be any cause/effect information. Like for the adenovirus example, how do we know that obese people (and people that are likely to become obese) aren't just also more likely to get colds?\n\nAlso, Re: post by shirley sommer - What evidence do you have for our hunter/gatherer forbears to not have suffered the diseases we have today? Seems to me that would be difficult to generate.\n\n

The obesity is most likely due to the food provided in the labs. A research study has shown the chow causes disease in the lab animals but when the chow is replaced by a chow prepared by the researchers themselves led to no disease PROVING there is 'something wrong' with the chow.\n\n"Mice maintained on defined iron-deficient diets, rather than chow diets, did not develope uroporphyria, even when the animals were\niron-supplemented either directly in the diet or by iron dextran injection."\n\nCoincidentally lipofuscin / fat is caused by iron.\n\n"Lipofuscin forms due to iron-catalyzed oxidation/polymerization of protein and lipid residues" \n